Our understanding of the cell biology of mitochondria has exploded in the last decade, providing a renewed understanding of their contribution to neurological diseases ranging from pediatric encephalomyopathies to Alzheimer’s, Huntington’s, and others.

Select faculty from the 2016 Neurobiology of Disease Workshop will continue the discussion, emphasizing mitochondrial motility and neurodegeneration, mitochondrial function in Alzheimer ’s disease, and the role of mitochondria in immunity and links to neuroinflammation. After the scientific presentations, join all the speakers here in the Neuronline Community for a live chat. Post your questions for the speakers in the replies below. *

In the live chat:

Heidi McBride, PhD, professor and Canada Research Chair in Mitochondrial Cell Biology at McGill University

Eric Schon, PhD, Lewis P. Rowland Professor of Neurology in genetics and development at Columbia University Medical Center

Xinnan Wang, PhD, assistant professor of neurosurgery at Stanford University School of Medicine

Want to learn more about neurobiology of disease?

We provide evidence that Alzheimer disease is functionally a disorder of ER-mitochondrial communication at contact sites between the two organelles (called mitochondria-associated ER membranes, or MAM), and that the biochemical cause of this altered ER-mitochondrial connectivity is perturbed lipid homeostasis.

Cells balance their energy homeostasis and minimize oxidative stress by regulating mitochondrial function and transport and by eliminating dysfunctional mitochondria. I will give a brief overview of mitochondrial motility and quality control and their implication in neurodegeneration and regeneration.

My presentation will focus on emerging roles for mitochondria in innate immunity and inflammation. I will briefly overview recent advances in the field and relate these findings to the pathobiology of mitochondrial and neurological diseases.

Usually they accumulate inside to a pretty high degree especially in the Hippocampus and Substantia nigra. Are you say you would not expect them to have an immunological effect unless they found their way to the membrane?

Question from registration:Mitophagy seems to have exploded from Pink1/Parkin to BNIP Optineurin NDP52 FUNDC3 etc. Are these redundancies or are there specific triggers to these pathways for e.g. pathological vs physiological mitophagy?

some studies suggests that membrane potential may affect the direction of mitochondria move, but other studies suggest otherwise. However, depolarization of membrane potential stops mito because Miro will be degraded.